2016 Fiscal Year Final Research Report
Establishment of ECM related Periodontal medicine
Project/Area Number |
26293437
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Partial Multi-year Fund |
Section | 一般 |
Research Field |
Periodontology
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Research Institution | Osaka University |
Principal Investigator |
Yamada Satoru 大阪大学, 歯学部附属病院, 講師 (40359849)
|
Co-Investigator(Kenkyū-buntansha) |
森崎 隆幸 国立研究開発法人国立循環器病研究センター, その他部局等, その他 (30174410)
竹立 匡秀 大阪大学, 歯学研究科(研究院), 助教 (60452447)
村上 伸也 大阪大学, 歯学研究科(研究院), 教授 (70239490)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Keywords | 歯周医学 / 遺伝子改変マウス / 細胞外マトリックス |
Outline of Final Research Achievements |
In this study, we investigated common molecules which are expressed and function in periodontal tissue and other organs/tissues to understand molecular pathogenesis of periodontal medicine. It was shown that PLAP-1 which is expressed in periodontal ligament and adipose tissue functions as positive regulator for adipogenesis. PLAP-1 KO mice shows the improvement of HFD-induced overweight and significantly high glucose tolerance and enhanced insulin sensitivity compared to WT mice. HFD-induced alveolar bone resorption in PLAP-1 KO mice were also less. In LDS model mouse, in which TGF-β signal is disordered alveolar bone loss by P.g inoculation was significantly increased, compared to WT. The LDS macrophages showed an up-regulated response to LPS compared to that of WT. These results suggest that PLAP-1 plays important roles in HFD-induced obesity and periodontitis and the abnormality of TGF-β signal may accelerate pathogenesis or progress of periodontitis.
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Free Research Field |
歯周病学
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